Document Detail

Hydrogen sulfide therapy attenuates the inflammatory response in a porcine model of myocardial ischemia/reperfusion injury.
MedLine Citation:
PMID:  19660398     Owner:  NLM     Status:  MEDLINE    
INTRODUCTION: Hydrogen sulfide is produced endogenously in response to myocardial ischemia and thought to be cardioprotective. The mechanism underlying this protection has yet to be fully elucidated, but it may be related to sulfide's ability to limit inflammation. This study investigates the cardioprotection provided by exogenous hydrogen sulfide and its potential anti-inflammatory mechanism of action.
METHODS: The mid left anterior descending coronary artery in 14 Yorkshire swine was acutely occluded for 60 minutes, followed by reperfusion for 120 minutes. Controls (n = 7) received placebo, and treatment animals (n = 7) received sulfide 10 minutes before and throughout reperfusion. Hemodynamic and functional measurements were obtained. Evans blue and triphenyl tetrazolium chloride staining identified the area at risk and infarction. Coronary microvascular reactivity was assessed. Tissue was assayed for myeloperoxidase activity and proinflammatory cytokines.
RESULTS: Pre-ischemia/reperfusion hemodynamics were similar between groups, whereas post-ischemia/reperfusion mean arterial pressure was reduced by 28.7 +/- 5.0 mm Hg in controls versus 6.7 +/- 6.2 mm Hg in treatment animals (P = .03). Positive first derivative of left ventricular pressure over time was reduced by 1325 +/- 455 mm Hg/s in controls versys 416 +/- 207 mm Hg/s in treatment animals (P = .002). Segmental shortening in the area at risk was better in treatment animals. Infarct size (percent of area at risk) in controls was 41.0% +/- 7.8% versus 21.2% +/- 2.5% in the treated group (P = .036). Tissue levels of interleukin 6, interleukin 8, tumor necrosis factor-alpha, and myeloperoxidase activity decreased in the treatment group. Treated animals demonstrated improved microvascular reactivity.
CONCLUSIONS: Therapeutic sulfide provides protection in response to ischemia/reperfusion injury, improving myocardial function, reducing infarct size, and improving coronary microvascular reactivity, potentially through its anti-inflammatory properties. Exogenous sulfide may have therapeutic utility in clinical settings in which ischemia/reperfusion injury is encountered.
Neel R Sodha; Richard T Clements; Jun Feng; Yuhong Liu; Cesario Bianchi; Eszter M Horvath; Csaba Szabo; Gregory L Stahl; Frank W Sellke
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-06-13
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  138     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-22     Completed Date:  2009-10-27     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  977-84     Citation Subset:  AIM; IM    
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MeSH Terms
Anti-Inflammatory Agents / therapeutic use*
Coronary Vessels / pathology,  physiopathology
Cytokines / metabolism
Free Radicals / metabolism
Hydrogen Sulfide / therapeutic use*
Microvessels / pathology,  physiopathology
Myocardial Contraction
Myocardial Infarction / pathology
Myocardial Reperfusion Injury / metabolism,  pathology*,  physiopathology
Myocardium / metabolism,  pathology
Peroxidase / metabolism
Grant Support
HL69024-02/HL/NHLBI NIH HHS; R01 HL046716/HL/NHLBI NIH HHS; R01 HL046716-17/HL/NHLBI NIH HHS; R01 HL069024/HL/NHLBI NIH HHS; R01 HL069024-07/HL/NHLBI NIH HHS; R01 HL085647/HL/NHLBI NIH HHS; R01 HL085647-02/HL/NHLBI NIH HHS; T-32HL076130-02/HL/NHLBI NIH HHS; T32 HL076130/HL/NHLBI NIH HHS; T32 HL076130-05/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Cytokines; 0/Free Radicals; EC; YY9FVM7NSN/Hydrogen Sulfide

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